Opportunistic gill infection is associated with TiO2 nanoparticle-induced mortality in zebrafish.

The large amounts of engineered titanium dioxide nanoparticles (TiO2NPs) that have been manufactured have inevitably been released into the ecosystem. Reports have suggested that TiO2 is a relatively inert material that has low toxicity to animals. However, as various types of NPs increasingly accumulate in the ocean, their effects on aquatic life-forms remain unclear. In this study, a zebrafish model was used to investigate TiO2NP-induced injury and mortality. We found that the treatment dosages of TiO2NP are positively associated with increased motility of zebrafish and the bacterial counts in the water. Notably, gill but not dorsal fin and caudal fin of the zebrafish displayed considerably increased bacterial load. Metagenomic analysis further revealed that gut microflora, such as phyla Proteobacteria, Bacteroidetes, and Actinobacteria, involving more than 95% of total bacteria counts in the NP-injured zebrafish gill samples. These results collectively suggest that opportunistic bacterial infections are associated with TiO2NP-induced mortality in zebrafish. Infections secondary to TiO2NP-induced injury could be a neglected factor determining the detrimental effects of TiO2NPs on wild fish.

The combined effects on neuronal activation and blood-brain barrier permeability of time and n-3 polyunsaturated fatty acids in mice, as measured in vivo using MEMRI.

N-3 polyunsaturated fatty acids (n-3 PUFA) are known to have cardiovascular and neuroprotective properties in both humans and rodents. Here, we use manganese-enhanced magnetic resonance imaging (MEMRI) to compare the effects of these polyunsaturated fatty acids on the combined effects of neuronal activity and integrity of blood-brain barrier integrity with saturated fatty acids from buttermilk. C57BL/6 mice (4 weeks old) were fed isocaloric diets containing 3% fish oil (3% FO, n=5), 12% fish oil (FO, n=6), 3% buttermilk (3% BM, n=6) or 12% buttermilk (12% BM, n=6) for 6 months. Following metabolic cage analysis these mice were scanned using a standard MEMRI protocol at 28-32 weeks of age. Adult mice aged 28-32 weeks old (RM3, n=5) and 15-16 weeks old (YRM3, n=4) maintained on standard rodent chow were also studied to assess age-related changes in brain barrier systems and neuronal activity. Signal intensity (SI) in the anterior pituitary (AP), arcuate hypothalamic nucleus (ARC), ventromedial hypothalamic nucleus (VMH) and the paraventricular hypothalamic nucleus (PVN) was significantly reduced in young compared to older mice fed standard chow. Furthermore, fish oil supplementation led to a decrease in SI within the ARC and PVN, reaching significance in the VMH in age-matched controls. Interestingly, both fish oil and buttermilk supplementation resulted in a significant increase in SI within the AP, a structure outside the BBB. We conclude that MEMRI is able to detect the combined effects of the integrity of neuronal activity and blood-brain barrier permeability in the hypothalamus associated with dietary manipulation and aging.

Impact of resistant starch on body fat patterning and central appetite regulation.

BACKGROUND: Adipose tissue patterning has a major influence on the risk of developing chronic disease. Environmental influences on both body fat patterning and appetite regulation are not fully understood. This study was performed to investigate the impact of resistant starch (RS) on adipose tissue deposition and central regulation of appetite in mice. METHODOLOGY AND PRINCIPLE FINDINGS: Forty mice were randomised to a diet supplemented with either the high resistant starch (HRS), or the readily digestible starch (LRS). Using (1)H magnetic resonance (MR) methods, whole body adiposity, intrahepatocellular lipids (IHCL) and intramyocellular lipids (IMCL) were measured. Manganese-enhanced MRI (MEMRI) was used to investigate neuronal activity in hypothalamic regions involved in appetite control when fed ad libitum. At the end of the interventional period, adipocytes were isolated from epididymal adipose tissue and fasting plasma collected for hormonal and adipokine measurement. Mice on the HRS and LRS diet had similar body weights although total body adiposity, subcutaneous and visceral fat, IHCL, plasma leptin, plasma adiponectin plasma insulin/glucose ratios was significantly greater in the latter group. Adipocytes isolated from the LRS group were significantly larger and had lower insulin-stimulated glucose uptake. MEMRI data obtained from the ventromedial and paraventricular hypothalamic nuclei suggests a satiating effect of the HRS diet despite a lower energy intake. CONCLUSION AND SIGNIFICANCE: Dietary RS significantly impacts on adipose tissue patterning, adipocyte morphology and metabolism, glucose and insulin metabolism, as well as affecting appetite regulation, supported by changes in neuronal activity in hypothalamic appetite regulation centres which are suggestive of satiation.